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Thursday, December 27, 2012

In the US, 27% of those aged 65 or
older have diabetes. Based on fasting blood glucose levels or glycated
haemoglobin levels, the estimate of the prevalence of pre-diabetes is 79
million cases. The economic cost has been estimated at around $2,000 per person
per annum. The maths aren’t complicated working out at about $22 billion per
annum. Most cases of type 2 diabetes are treated
initially by lifestyle changes and then by drugs to manage blood glucose. In
2009, the American Diabetes Association defined partial remission from diabetes
when fasting blood glucose levels were lowered to below the diagnostic norm and
complete remission when fasting blood glucose levels returned to normal, in
both cases in the absence of drug therapy. Relatively little is really known of
the extent to which such partial or complete remission can be achieved with
lifestyle interventions. In 2001, a large multicenter study was established in
the US known as “Look Ahead”, (Actions for Health in Diabetes)[1].
The trial, funded by the National Institute of Health, involved 2,262 type 2
diabetics given a basic diabetes lifestyle intervention and a group of 2,241
type 2 diabetics given an intensive lifestyle intervention. The former were
given 3 group sessions per year while the latter participated in weekly group
and one-on-one counseling for the first 6 months followed by 3 sessions per
month for the next 6 months and twice monthly sessions thereafter. For this
group, a target caloric intake was set between 1,200 and 1,800 calories per day
with an exercise goal of 175 minutes of moderately intensive exercise per week
(25 minutes per day). The Look Ahead
trial laid out its hypothesis quite clearly: that there would be a significant
reduction in heart disease and stroke in the intensively counseled group
compared to the group receiving standard advice on lifestyle. The trial has
produced over 80 peer reviewed papers and has shown that intensive lifestyle
intervention can significantly improve body-weight, blood pressure, blood
glucose control and blood lipid levels.

On October 19th this year, when the
trial was well into its 11th year, the NIH announced the end of the trial on
foot of recommendations from the trial’s data and safety monitoring board. This
independent body of experts noted that despite the above improvements on risk
factors for cardiovascular disease, there was no statistically significant
difference in cardiovascular events between the two groups which was the
central hypothesis. Recently, the trial study group published a paper in the
Journal of the American Medical Association showing that intensive lifestyle
intervention did indeed lead to a greater rate of remission of type 3 diabetes
compared to the standard intervention[2].
The big disappointment was, however, that the impact of intensive lifestyle was
very small. The rate of partial or complete remission in year 1 was 11. 5% in
the intensively tutored group, falling to 7.3% at year 4. In contrast, the
group receiving standard counseling showed a 2% reduction at both time points.
Very clearly, type 2 diabetes is not a reversible condition for the vast
majority of subjects. And just as clearly, this low response rate in correcting
diabetes pathologies explains why no differences in heart disease were observed
between the two treatment groups.

In the same issue of this journal,
an editorial looks at the overall evidence for lifestyle and surgical
interventions in obesity[3].
The latter are usually confined to subjects with very severe cases of obesity.
The latter leads to type 2 diabetes remission rates, which are 12 to 24 fold
greater than intensive lifestyle interventions. The Swedish Obesity Study, also
published in this year’s JAMA, reported on the long-term effects of the
surgical treatment of obesity. Subjects were morbidly obese at baseline (1987
was the start date) and the average duration of follow up was 14.7 years[4].
Compared to conventional medical and lifestyle treatment, the surgical
intervention reduced fatal heart attacks by 47%, all heart attacks by 52% and
stroke by 34%. Surgery is expensive but so too is intensive lifestyle
interventions and thus some cost comparisons between the two would be
interesting.

Clearly, we are in a mess and we
must now live with the mess. But how can we prevent the mess for future
generations?. Whilst 79 million Americans have prediabetes and are at risk of
developing diabetes, the remaining 233 million don’t. Of those aged over 65
years, 11.2 million have type 2 diabetes while the remaining 30 million over
65s do not. They all live in the same obesogenic US environment. One day, not
far from now, we will be able to predict who is likely to to draw the short
straw and develop obesity-related type 2 diabetes. Moreover, this genetic
information will soon be able to zone in on that aspect of diet and lifestyle,
which is most responsible for the development of diabetes. For some, it may be
a metabolically based genetic factor. For others, it may be a food choice
factor that is the driver and for others it may be a defective satiety system.
Understanding personal risk and understanding personalised solutions is the
future for nutrition and health. In the meantime, we have a mess.

Tuesday, December 11, 2012

In the obesogenic environment that we live in, not everyone
becomes obese. To the high priests of nutrition, that variability is put down
to variation in self-control and self-discipline and that in turn relates to
level of education and social class. The idea that this variation might be
genetically based is dismissed with the old reliable falsism that since our
genes have not changed during the recent epidemic of obesity, it’s the
environment that counts. Well, yet another twin study shows that this is
nonsense and this twin study is somewhat special since it pooled data from 23
twin cohorts from four countries: Denmark, Australia, Canada and Sweden
involving just over 24,000 children[1].
Moreover, this pooling study was able to provide data on twins from birth
through 19 years of age. By comparing variation within and between both
identical and non-identical twins, it is possible to distinguish the effect of
genes from the effect of the environment and the latter can be split into common
and unique environments. At birth, only 8% of variation in weight or body mass
index (BMI) could be explained by genetic factors. By 5 months this had
increased to 65% and rose into the 70% decile up to 9 years of age. In the
early teens the genetic variation had reached into to 80% decile and by late
teens it had hit 90%. As children got
older, the environmental explanation of obesity had fallen from 74% at birth,
to 25% at 6 years and down to about 10% in late teens. While this study clearly
shows the powerful effect of genetic factors on obesity, it does raise the
question as to why this genetic dimension increased with age. Clearly, the
genetic make up remained constant so most likely, changes in gene expression
were the contributory factor. Growth in childhood and especially in adolescence
is associated with significant biological adjustments, which could create the
environment for altered gene expression.

One of the reasons which I personally think public health
nutritionists are wary of the genetic influence on obesity is that the subject
is strongly orientated toward basic biology, effectively, the digestion,
absorption, transport, distribution and utilisation of calories from fat,
carbohydrate, protein and alcohol. However, genetic influences on behaviour are
to my mind far more important than the
genetics of basic biological elements. A recent twin study has looked at the
heritability of taste[2]. Subjects were given a strawberry jelly with
or without the hot spice capsaicin derived from chili peppers. They were also
asked questions on their liking or otherwise of spicy foods and spices and of
foods that have mild, strong and extremely strong pungency properties. 50% of
the variation in preference for spicy foods and spices and 58% of the variation
in “pleasantness of strong pungency” was explained by genetic factors. Another
twin study looked at food neophobia in a group of children aged 8 to 11 years,
comprising 5,390 pairs of identical and non-identical twins[3]. Parents were asked about their children’s
attitude to foods with four statements: “My child is constantly sampling new
and different foods”, “My child doesn’t trust new foods,” “My child is afraid
to eat things/he has never had before.” and “If my child doesn’t know what’s in
a food s/he won’t try it.” A food neophobia score was worked out and the highly
robust finding of the study was that a staggering 78% of variation in food
neophobia was genetic in origin. Only 22% was learned from the environment.
These studies show that the genetic component of obesity need not be related to
the biochemistry of energy metabolism, but rather to more complex behavioural
traits such as food choice.

Twin studies of obesity always raise the question of
assortative mating, that is fat partners mating with other fat partners and
similarly for slim partners. Assortative mating has been shown to occur in
personality type, education, religion, politics, age, smoking habits and
anti-social behaviour. Researchers at the Rowett Institute in Aberdeen used
DEXA scans to accurately measure body fat levels in 42 couples[4].
Strong evidence for assortative mating in relation to body fat was found. For
example, subjects with disproportionately large arms assortatively mated with
like partners. Given the high heritability of the propensity to develop obesity,
assortative mating will accelerate the incidence of obesity sine the children
of such parents are likely to inherit genetic patterns from both parents.

The high priests of public health nutrition may dislike the
implications of a genetic dimension to obesity but they are being increasingly
isolated from the scientific truth.

Thursday, November 15, 2012

The Danish
government has abandoned its tax on fat and and its plans for a sugar tax.A spokesperson for the tax ministry is quoted
thus: “The suggestions to tax foods for
public health reasons are misguided at best and may be counter-productive at
worst.Not only do such taxes not work,
especially when they choose the wrong food to tax, they can become expensive
liabilities for the businesses forced to become tax collectors on the
governments behalf”[1].
Shortly we will have our annual budget here in Ireland and notwithstanding
the volte-face of our Danish colleagues, the likelihood is that we will face
such a tax soon.In general, the
predicted weight changes associated with projected taxes on sugar sweetened
beverages are grossly overestimated.

A recent
consensus statement of the American Society of Nutrition (ASN) and the
International Life Sciences Institute (ILSI) has examined the topic:“Energy
balance and its components:Implications
for body weight regulation”[2].One of the areas covered by this paper is the
popular and widely held belief that to lose 1lb of body weight, you need to
reduce caloric intake by 3,500 kcal.This figure assumes that a loss of 1lb of body weight is made up
entirely of adipose tissue which is 86% fat and the fat has 9 kcal per
gram.This 3,500 kcal figure is widely
used in predicting the benefit of weight loss from a sugar sweetened beverage
tax.It has many flaws.

Firstly, a 1lb
weight loss will not be 100% fat but will also involve the loss of some lean
tissue (muscle and protein elements of adipose tissue and its metabolism).Whereas fat has an energy value of 9 kcal/g,
lean tissue has a value of 4 kcal/g.The
exact ratio of the loss of lean and fat in weight reduction depends largely on
the level of fat in the body at the outset.The higher the intake level of fat, the higher the proportion of fat
lost.However, as a person sheds fat,
the ratio of fat to lean changes in favour of the latter, so subsequent weight
loss will have a lower ratio of fat to lean.The blanket use of the 3,500kcal value ignores this.

The second
criticism of this rule is that it ignores time.If you shed 3,500kcal per week every week, that would differ from a
deficit of 3,500 kcal per month every month.The former leads to a daily deficit of 500 kcal while the latter is just
117 kcal.Even the most non-expert
dieter knows that such differences in daily energy deficits will lead to
radically different rates of weight loss.Thirdly, the 3,500 kcal rule assumes complete linearity – in other words
the rule equally applies, pound after pound of weight loss. We saw above that
progressive weight loss will progressively increase the % of that weight loss
as lean tissue but more importantly, the 3,500kcal rule ignores a major
adaptation in energy expenditure.Basically, our basal metabolic rate (BMR) falls as we restrict our
caloric intake.Since BMR accounts for
88% of energy expenditure in most sedentary persons, that means that a fall in
BMR represents a significant adaptive response through increased efficiency of
energy use making weight loss progressively more difficult.

Researchers at
the US National Institute of Health have developed a very detailed mathematical
model which predicts weight loss based on a wide variety of inputs[3].The model has been validated against a number
of highly controlled weight loss programmes.Together with researchers based at the USDA and the economics
departments of the universities of Florida and Minnesota, they have examined
the likely weight loss that would accrue from a tax of 20% (about 0.5 cents per
ounce) on sugar sweetened beverages in the US[4].They concluded that the nutritional input
would be a reduction of energy intake of 34-47 kcal per day for adults.Using the 3,500 kcal rule, an average weight
loss of 1.60kg would be predicted for year 1 rising to 8kg in year 5 and to
16kg in year 10.However, when the
dynamic mathematical model is used, the corresponding figures for years 1, 5
and 10 are, respectively, 0.97, 1.78 and 1.84 kg loss.The % of US citizens that are over-weight is
predicted to fall from existing levels of 66.9% over-weight to 51.5%
over-weight in 5 years time using the 3,500 kcal rate but using the dynamic mathematical
model, the 5-year figure for the over-weight population in the US would be just
62.3%.Clearly, the continued use of the
3,500 kcal rule in predicting weight loss should cease and the recommendations
of the consensus statement of the ASN and ILSI should apply: “Every permanent 10 kcal change in energy
intake per day will lead to an eventual weight change of 1lb when the body
reaches a new steady state.It will take
nearly a year to achieve 50% and about 3 years to achieve 95%”.

My back of
envelope calculations based on the National Adult Nutrition Survey is that
extrapolating from the US model (footnote 4), a tax on sugar sweetened
beverages might lead to a weight loss of 0.6 lb at the end of year 1. That of
course is subject to an error estimate such that it might be higher but
equally, it might be lower. Many of the advocates of fat taxes might argue that
they will take that “thank you very much” as a start and then move to the next
food. But you cannot continue to add tax to the cost of food.

Tuesday, October 30, 2012

Sometime back in the early 1990s or thereabouts, Dolly Parton was
being interviewed by the famous BBC chat show host, Michael Parkinson. When
asked about what diet she used to keep her figure, she replied: “Honey, if you
want to lose weight, get your head out of the slop bucket”. In other word, just eat less. No truer
words were ever uttered in the vast realm of advice on dieting. This year we
have seen a number of scientific papers published on sugar sweetened beverages,
some designed to boost weight gain and some designed to induce weight loss, all
adding to the belief that sugar sweetened beverages are both the cause and the
cure for modern obesity. A recent paper from the Department of Nutrition at
Harvard will help put things in perspective, but only for those wishing to have
an accurate perspective.

The first [1] of the sugar
papers looked at four groups each given 1-liter of a beverage per day for 6
months. Group 1 receiver a liter of regular sugar sweetened Coke. Group 2 were
given a liter of semi-skimmed milk with an approximate equal calorie level to
the Coke. Groups 3 and 4 respectively received 1 liter of diet Coke or water.
According to the authors, the consumption of the energy-containing beverages
led to a compensation effect with a reduction in the intake of other foods and
no overall change in energy intake. No dietary data are provided in the paper
but 1 liter of regular Coke would have diluted out its equivalent caloric value
from all other foods, leading to a reduction in the intake of the latter by 430
calories per day. This Coke group showed a significant accumulation of fat in
the liver compared to others but we will never know if it was due to the
absurdly high total intake of sugars (about double the normal according to my
calculations) or to a reduction in the intakes of micro-nutrients associated
with 430 less food than normal every day. Coke for example, does not contain, the
B-vitamin riboflavin, but low riboflavin status will lead to increased blood
pressure, and the authors did see a rise in blood pressure with regular
Coke.

So, 1 liter of Coke per day did not lead to weight gain ( for example
a 1.3% gain with Coke and a 0.8% gain with water). However, two studies
reported in the New England Journal of Medicine show that if sugar sweetened
beverages in children are replaced with a calorie free version, then weight
loss does occur [2]. These
studies will be widely cited as evidence that sugary drinks cause obesity. In
fact, these studies simply show that if you do as Dolly Parton says, and simply
eat less, you will lose weight so the weight loss could have been with any
caloric source, not just sugar-sweetened beverages.

Which brings me to the Harvard paper [3].
This study (a subset of a larger dietary intervention) looked at how variation
in the distribution of calories in a weight loss regimen influenced weight
change and also changes in body composition. Four dietary treatments were used
and an energy deficit of 750 kcal per day was the target for each participant.
The diets varied the level of fat, protein and carbohydrate. At 6 months, the
average amount of fat lost was 4.2 kg and the loss of lean tissue was 2.1
kg. About half of this fat loss
was due to loss of fat from the abdominal fat with about a third lost from
subcutaneous fat. Only 0.1 kg of fat was lost from the liver but this
represented a loss of 16% of liver fat. There were no differences in any of
these measures according to the composition of the weight reduction diets,
again, upholding the Dolly Parton rule.

In summary, the first study tells us that if you oblige subjects to
eat a 1-liter bottle of regular Coke every day, you won’t gain weight because
you reduce your intake of other foods keeping energy intake constant. The
second tells us that extracting calories from children’s diets will lead to a
weight loss, in this case using sugar sweetened beverages as the target food.
The third tells us that Dolly Parton was correct. It really doesn’t matter what
the composition of your weight reducing diet is so long as the caloric
restriction operates.

So for what its worth, here are my basic rules about successful
dieting:

1.Never start a diet until you have though
about it long and hard given that the relapse rate of weight loss is so high.

2.Never start a diet until you have built
physical activity into your daily routine. Physical activity will reverse the
negative effects of obesity such as poor glucose management, higher blood
pressure and elevated blood lipids.

3.Don’t diet on your own. Join a weight loss
group and get the benefit of the social network of dieting and maintaining
weight loss.

4.Heed Dolly Parton and just eat less and
eat according to your preferences

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"Ever seen a fat fox ~ Human obesity explored"

About Me

I graduated from University College Dublin in 1971 with an Masters in Agricultural Chemistry, took a PhD at Sydney University in 1976 and joined the University of Southampton Medical School as a lecturer in human nutrition in 1977. In 1984 I returned to Ireland to take up a post at the Department of Clinical Medicine Trinity College Dublin and was appointed as professor of human nutrition. In 2006 I left Trinity and moved to University College Dublin as Director of the UCD Institute of Food and Health. I am a former President of the Nutrition Society and I've served on several EU and UN committees on nutrition and Health. I have published over 350+ peer reviewed scientific papers in Public Health Nutrition and Molecular Nutrition and am principal investigator on several national and EU projects (www.ucd.ie/jingo; www.food4me.org). My popular books are "Something to chew on ~ challenging controversies in human nutrition" and "Ever seen a fat fox: human obesity explored"